CVD Flashcards
Endocarditis Sx
Fever, New Murmur, Janeway lesions (nontender on palms/soles), Osler’s nodes (tender nodules of finger/toe pads), Roth spots (red retinal lesions w. pale centers
Endocarditis Dx
Modified Duke Criteria
TEE
positive blood cultures
Endocarditis Tx
Empiric tx = vancomycin + ceftriaxone Prosthetic valve = add rifampin & gentamicin
Arrhythmias
An abnormality in the timing or pattern of the heartbeat caused by a variety of things
Brady or tachy
Cardiac Tamponade Sx
Becks triad: hypotension, JVD, muffled heart sounds
Becks triad
Hypotension, JVD, muffled heart sounds
Cardiac tamponade Dx
EKG: Sinus tachy, low voltage, electrical alternans
POCUS triad (US): Pericardial fluid, RV diastolic collapse, Dilated IVC
Cardiac Tamponade Tx
Pericadiocentesis
Chest Pain
Nonspecific, can be caused by a variety of disorders like MI’s, anginas, pneumonia, PE
AFib Dx
EKG: No identifiable P waves, varying R-R intervals
AFib Sx
Unexplained fatigue, palpitations, fainting, SOB, chest pain, stroke (common from left atrial appendage)
AFib Tx and management
Anticoagulation: rivaroxaban, apixaban, dabigatran, edoxaban, warfarin, heparin
Rate control – older, preserved EF, asymptomatic. Rx = BB, CCB
Rhythm control – younger, symptomatic, EF <45%, new onset
Cardioversion or ablation if the above doesnt work
CHA2DS2-VASc
Anticoagulation if score is 2+.
1 pt: CHF, HTN, DM, Vascular disease (MI, PAD, atherosclerosis), age 65-74, female
2 pt: age 75+, stroke/TIA
Atrial Flutter dx
EKG: Produces a classic “sawtooth” pattern of atrial activity with lack of P waves
Atrial Flutter Tx
Anticoagulation
Cardioversion, if hemodynamically unstable
SVT definition
Rapid rhythm disturbances originating from the atria or the atrioventricular node (narrow complex)
SVT Sx
Abrupt onset, heart racing/palpitations, SOB, diaphoresis, chest pain, rapid breathing, dizziness, loss of consciousness
SVT dx
EKG: narrow QRS complex, usually 160-220 bpm, rate does not vary
SVT Tx
Physical maneuver if isolated incidences (valvsalva, hold breath, head btw knees, ice water)
IV Adenosine (in acute setting) Only give adenosine if narrow QRS
Send for EP study (stable), cardiovert (if unstable)
Ablation (definitive treatment)
LBBB vs RBBB
LBBB= wide QRS (>0.12s), will have –> think batman
RBBB = left ventricle depolarizes first, then right (b/c that’s where delay is) –> think rabbit ears
V1, V2 = RBBB
V5, V6 = LBBB
VTach EKG findings and Sx
EKG: Wide QRS (>120ms) originating from ventricles (rate >100)
Sx: May present as syncope +/- hemodynamic stability
VTach Tx (initial vs long term)
Initial: Urgent cardioversion, IV amiodarone
Long-term: reverse cause, BB if structural heart disease, ablation, ICD if cardiomyopathy/EF<35% after GDMT
Torsades de pointes causes, EKG findings, and Tx
Cause: commonly hypomagnesemia if electrolyte disturbance
Clinical Pearl: Prolonged QT interval = higher risk of developing polymorphic VT
Tx: IV magnesium
VFib EKG findings and tx
What happens to ventricles during VFib?
Main cause of sudden cardiac death in pts w. MI
Ventricles quivering w. no forward cardiac output
EKG: Chicken scratch
Tx: ACLS (defibrillation, epinephrine, antiarrhythmics)
PVC definition
Premature, ectopic, wide complexes, compensatory pause
PVC Sx
Most asymptomatic, can feel heart skip a beat
What are PVC’s associated with?
May be associated w. caffeine, energy drinks, stress, electrolyte abnormalities, hyperthyroidism
PVC tx (symptomatic vs asymptomatic)
Asymptomatic: None
Symptomatic: 1st line is beta-blockers or non-dihydropyridine CCB.
PAC definition
An extra heartbeat that occurs occasionally, often for no known reason, momentarily throwing off the heart’s normal rhythm
STEMI labs
Positive troponin or CK-MB
Positive as early as 4-6 hrs after MI onset, abnormal by 8-12 hrs
May remain elevated 5-7 days+
CK-MB generally normalizes w/in 24 hrs
STEMI EKG
Peaked “hyperacute” T waves
ST-segment elevation
Q wave development or old infarct
T wave inversion
New LBBB – considered STEMI equivalent until proven otherwise (reference old EKGs)
STEMI Sx
Chest pain
Shortness of breath or trouble breathing
Nausea, stomach pain or discomfort
Heart palpitations
Anxiety or a feeling of impending doom.
Sweating.
Feeling dizzy, lightheaded or fainting.
Anterior wall MI: EKG leads and location in heart
Think about septum & left ventricle
V2-V4: anterior wall
LAD (affects LV = more prone to LV heart failure)
Prone ventricular arrythmias/ shock
Lateral wall MI: EKG leads and location in heart
I, aVL, V5, V6
Left Circumflex Artery
Inferior wall MI: EKG leads and location in heart
Think right ventricle & SA/AV node
II,III,aVF
Right Coronary Artery
Give IV fluids
Pre-load dependent = caution w. nitro & morphine
Tx of STEMI, NSTEMI and unstable angina
MONA-BAS
Morphine – chest discomfort after NTG; watch bp/pulse
Oxygen – supplemental
Nitroglycerine
Aspirin – 162-325 mg loading dose
Beta blockers (oral, IV. Watch BP/HR)
Antiplatelet (Clopidogrel, prasugrel, ticagrelor)
Anticoagulation (Heparin: enoxaparin [lovenox] or unfractionated heparin) per doctor in ER if troponin is (+) add heparin
Statin (Atorvastatin, rosuvastatin)
+/- cath
Stable Angina definition and sx
Chest wall discomfort precipitated by stress or exertion and relieved by rest or nitrates
Sx: pressure, pain, squeezing, tightness, heaviness…
Sx’s are EXERTIONAL and RELIEVED WITH REST
<20 minutes duration
Stable angina labs and imaging
Negative troponin/CK-MB
EKG: Resting EKG is often normal. Possible Ischemic changes: ST depression, T wave flattening or inversion
Stress test w or w/o imaging (myocardial perfusion scan or stress echo)
Cardiac CTA
Stable angina Tx
1st line: Beta-blockers – prolongs life (first line therapy)
Aspirin 81-325 mg or clopidogrel 75 mg
2nd line: long acting nitrates
Unstable anginas/NSTEMI CP typically lasts (GREATER/LESS) than ____ minutes
Greater than 30 minutes
What differentiates an NSTEMI vs unstable angina?
Positive troponin in NSTEMI
EKG findings in unstable angina/NSTEMI
ST depression
What is the criteria for ST elevation on EKG?
ST segment must be elevated greater than 2 mm (aka greater than 2 small boxes)
What medication will you give in a STEMI but NOT an NSTEMI?
Fibrinolytic therapy
Definition of Prinzmetal’s/Variant Angina + what causes it
Known as coronary vasospasm
Angina pain usually at rest (often b/w midnight-early morning) with no change in exercise function
More common in women < 50
May be induced by exposure to cold, emotional stress, or vasoconstricting medications
Usually involves right coronary artery (RCA)
EKG findings in Prinzmetal’s/Variant Angina
ST elevation- gets confused for STEMI
How to dx Prinzmetal’s/Variant Angina and how to tx
Dx: EKG and CTA
Tx: CCB and/or nitrates
Definition of DOE
Difficulty breathing that is elicited with physical activity. Presents in a variety of CVD and pulm disorders
Definition of edema
Swelling caused by fluid trapped in your body’s tissues
Typically seen in LE dt gravity
Can be seen dt infection/inflammation
Sx of CHF
DOE, SOB, orthopnea, edema, abdominal bloating/distention, cough, decreased appetite
Differentiate right vs left sided CHF
Left-sided:
Rales/crackles/wheezes
Dullness to percussion
S3, S4 or gallop
Right-sided:
Distended neck veins, elevated JVP (>8 cm)
Abdominal distention
Pedal edema (1-4+)
Hepatojugular Reflux
Ascites
Liver enlargement/tenderness
CHF labs and Dx
Labs: BNP, CBC, CMP
Dx: Echo, EKG, CXR
What CXR findings can be seen in CHF?
A: Alveolar edema (bat wing opacities)
B: Blunting of margins, Kerley B lines
C: Cardiomegaly
D: Dilated upper lobe vessels
E: Pleural effusion, Pulmonary edema
CHF tx
BASS
SGLT2-I
ARNI/ACE/ARB
Spironolactone (MRA)
BB (metoprolol or carvedilol)
Furosemide if wet CHF
What are EKG findings in Atrial enlargement/hypertrophy (RAE/LAE)? What lead should you look at?
Look at lead 2
RAE: taller P wave (kinda looks like mountain with small notch)
LAE: wider, notched P wave (looks like 2 boobs)
Hypertensive urgency vs emergency
Goal reduction
BP presenting
Signs/Sx
Tx
Urgency:
Goal: reduce BP in hours
BP: >180/120
Signs/Sx: +/- HA/CP, NO evidence of end organ damage
Tx: outpatient po – ACTS meds
Emergency:
Goal: Reduce BP 10-20% in 1 hour
BP: >180-220/120
Signs/Sx: Evidence of end organ damage
Tx: inpatient IV (labetalol)
EKG findings of LVH
Larger S in V1, larger R in V5 (if greater than 35 mm = LVH)
Seaman’s sign: R waves touch S waves
T waves typically inverted
EKG findings in RVH
Reverse R wave progression
Normally R wave increases V1 –> V6
RVH: Larger R wave and smaller S in V1
Cardiogenic hypotension: definition, causes, Sx and Tx
Volume maintained, decreased CO, incr. resp. effort
MI, myocarditis, valvular disease, congenital heart disease, cardiomyopathy, arrhythmias
Sx: Decrease cardiac output, hypotension, vasoconstriction (incr. SVR)
Tx: Oxygen, fluid resuscitation
Orthostatic hypotension causes and Sx
Aka postural hypotension
Hypotension when standing up after sitting/laying down
Can be dt blood loss, vasodilators, diuretics
Sx:
* Lightheadedness or dizziness upon standing
* Blurry vision
* Weakness
* Fainting (syncope)
* Confusion
How to manage orthostatic hypotension (medication vs non medication)
Non medical Management:
* External compression devices such as waist-high compression stockings
* Physical maneuvers such as lunges, calf-raise, squatting, leg crossing
* Increase water and fluid intake to about 2-3 liters per day, avoid dehydration
* Increase salt in diet 6-10g/day
* Raising the head of the bed to 10 degrees at night
Medication Management: Goal = incr. blood volume
* Midodrine 2.5 to 15mg PO QD to TID
* Fludrocortisone 0.1 to 0.2mg daily in AM titrated up to 1mg daily PRN
* Pyridostigmine 30 to 60 mg PO TID
* Yohimbine 5.4 to 10.8mg PO TID
* Octreotide 12.5 to 50 ug subcutaneously BID
* Cafergot such as caffeine 100mg and ergotamine 100mg
DONT NEED TO KNOW MEDICATIONS (probably)
Definition of orthopnea and how to relieve it
o SOB whilst laying down
o Relieved by sitting up
o Typically seen in CHF, pericarditis, Pericardial effusion/tamponade, pleural effusion
o Tx underlying cause
Pericardial effusion definition and Sx
Definition: Extra fluid in pericardial space creates pressure on heart chambers
Sx:
Asymptomatic (depends on size/effect)- incidental finding
Constant dull ache, tachycardia, hypotension, JVD, Pulsus paradoxus (blood pressure decreases with inhalation), dysphagia, dyspnea,
Becks triad
* Muffled heart sounds
* Increased JVP
* Hypotension
Dullness to percussion L lung over angle of scapula (Ewart’s sign)
Pericardial effusion Dx (and their findings) and labs
Labs: CBC, CMP, BNP, ANA
Dx:
EKG: low QRS voltage with sinus tach, electrical alternans
CXR: enlarged cardiac silhouette with clear lungs
Can do echo to quantify effusion and assess hemodynamic impact
PVD/PAD causes, RF, and clinical findings
Systemic atherosclerosis
Risk Factors: CAD, HTN, male, dyslipidemia, incr. age. Diabetes, metabolic syndrome, tobacco use
Clinical Findings
Intermittent claudication
Cramping pain in the lower extremities
Induced by activity, relieved with rest
Cool skin temperature
Pale skin color
Scant hair distribution
Weak distal pulses
Nonhealing wounds
How to dx and manage PAD/PVD
Dx: Ankle Brachial Index (ABI) (an ultrasound)
* Normal: 1.0-1.4
* PAD: < 0.90
* Severe disease: < 0.5
CT angiography (Gold standard) or MRA
Management
Antiplatelet Therapy
Clopidogrel
Aspirin
High-intensity Statin Therapy
Risk factor modification
Sx of syncope
Lightheadedness.
Feeling unstable in the upright position.
Warm or cold/clammy.
Sweating.
Palpitations
Nausea, vomiting, or nonspecific abdominal discomfort.
Visual “blurring”
Differentiate between vasovagal syncope, carotid sinus hypersensitivity, cardiogenic syncope, and situational syncope. How do you manage/tx?
Vasovagal syncope - “common faint. Caused by stressful, painful, or claustrophobic experience
Carotid sinus hypersensitivity: Stimulation of abnormally sensitive carotid body, with subsequent abnormal vagal response. Results in bradycardia and arterial relaxation/dilation
Situational syncope: Enhanced vagal tone with resulting hypotension. Coughing, sneezing, micturition, exercise
Cardiogenic syncope: Mechanical or arrhythmic basis arising from heart. Brady: Sinus brady, sinus pauses, AV block
Tachy: Ventricular tachycardia
Mechanical: Aortic stenosis, Pulmonary stenosis, hypertrophic cardiomyopathy, congenital lesions, massive PE
Tx:
Trigger avoidance
Increase fluids and salt
Compression stockings
Counterpressure maneuvers – Reduce venous pooling & improve cardiac output or move to supine position
Leg-crossing with simultaneous tensing of leg, abdominal, and buttock muscles (very effective).
Handgrip – maximum grip on a rubber ball or similar object
Aortic stenosis:
Sx
PE
Dx
Tx
Narrowing of aortic valve
Sx: asymptomatic, SAD (syncope, angina, dyspnea), HF result of LV dysfunction
PE: Harsh crescendo-decrescendo systolic murmur (heard best@ RUSB)
S1 is usually unaffected, as AS progresses S2 diminishes and can eventually disappear
Dx: TTE, EKG (can be normal, LVH, left atrial enlargement)
Tx: Valve replacement, Lifelong anticoagulation, TAVR
Aortic regurgitation causes (acute vs chronic), Sx, PE, Tx
Causes:
* Acute: Infective endocarditis, Marfan’s syndrome, Aortic dissection*, Acute prosthetic valve dysfunction, Inflammatory disease, Dilated CM
* Chronic: bicuspid valve, dilated CM
Sx: Asymptomatic, Exertional dyspnea, Fatigue, Atypical chest pain, Eventual LV dilation & failure, Orthopnea/PND
PE: Displaced PMI lateral to midclavicular line in 5th intercostal space
Diastolic thrill maybe palpable in 2nd left intercostal space
* Wide pulse pressure (big difference in SBP and DBP)
* Water Hammer Pulse: Collapsing pulse. Rapid swelling & falling arterial pulse. Best on radial/brachial/carotid pulses.
* Corrigan Pulse: Similar to water hammer but referring to carotid artery
* Hill’s Sign: Popliteal cuff systolic pressure > brachial pressure by more than 60 mmHg while recumbent. Most sensitive for AI.
* Muller’s Sign: visible systolic pulsations of the uvula
* De Musset’s Sign: Head-bobbing with each heartbeat
* Becker’s Sign: Visible pulsations of retinal arteries & pupils
* Rosenbach’s Sign: Systolic pulsations of liver
* Gerhard’s Sign: Systolic pulsations of spleen
Tx:
Mild: vasodilators (hydralazine), diuretics, BB, CCB, ACE
Severe:
Surgery: TAVR, aortic root replacement
Mitral regurgitation Sx (acute vs chronic), PE, Dx, Tx
Sx:
Acute MR: sudden onset SOB, orthopnea, LE edema, possible cardiogenic shock
Chronic MR: asymptomatic for yrs, then exertional dyspnea & intolerance. Fatigue, orthopnea & PND as MR progresses. Palpitations: possible atrial fibrillation as a result of LA dilation
PE:
High-pitched blowing Holosystolic murmur
Heard best at apex (may radiate to axilla)
Possible S3
Dx:
Echo (regurgitant volume, EF, LA/LV size, PA pressure, RV function)
BNP (early identifier of LV dysfunction)
CXR (acute vs. chronic MR)
Tx:
Meds:
o Vasodilators: hydralazine, ACE
o Diuretics
o Anticoag if Afib
Surgery
* Acute severe MR (urgent): stabilize w. vasodilators to incr. pulm. Pressure & maximize forward flow
* Chronic severe MR (elective): if reduced EF or LV dilation w. reduced contractility
Abdominal Aortic Aneurism who to screen
90% originate below renal arteries
Involvement of the aortic bifurcation
Screening:
o Abdominal ultrasound
o Men 65-75 years-old
o Family history (1st degree relative)
o Smoking history (current or past)
Abdominal Aortic Aneurism clinical findings (asymptomatic vs symptomatic)
Asymptomatic: Incidental finding on abdominal ultrasound or CT imaging
Symptomatic: Sign of rapid expansion or impending rupture
Mild to severe deep abdominal or flank pain that is constant or intermittent
Exacerbated upon palpation
Pain radiates to back
Risk of AAA rupture increases drastically when diameter is > _____
Risk of AAA rupture increases drastically when diameter is > 5.5 cm
AAA initial screening vs assessing diameter
initial: US
assessing: Abdominal CT w. contrast to assess diameter & for surgical planning
When to refer for surgical repair for AAA
o Diameter > 5.5 cm
o Rapid diameter expansion (> 0.5 cm in 6 months)
o Symptomatic – Pain, tenderness
What are clinical findings of a TAA
Symptoms dependent upon size & position of aneurysm & rate of growth
Esophagus: dysphagia
Trachea: stridor, dyspnea
Superior vena cava: Upper extremity edema, JVD
Aortic root: Aortic regurgitation
Substernal chest pain
Pain radiating to the back or neck
What imaging is used to determine a TAA
Chest radiographs: useful initial evaluation, not sensitive or specific
CT Angiography: Best initial imaging for patients suspected to have TAA
TEE or TTE
Surgical indications for TAA
Diameter > 5.5 cm
All symptomatic TAAs require surgical repair
An aortic dissection occurs when there is a spontaneous tear of the ____ _____
Spontaneous tear of tunica intima
What is the number one cause of aortic dissection?
HTN
Clinical findings of aortic dissection
- Sudden onset severe, persistent chest pain described as ripping, sharp, tearing
- Pain radiates in respect to location & extent down the back, anterior chest and/or neck
- Hypertension
- Syncopal episodes
- Diminished peripheral pulses
- Variations in pulses and blood pressure when comparing extremities
Aortic dissection imaging
EKG
Chest Radiograph (x-ray): Widening of mediastinum/aortic silhouette
CT of chest & abdomen: Immediate diagnostic imaging of choice
TEE
Aortic dissection tx and management
Surgical Repair
Management and Disposition
* Aggressive blood pressure control
o Reduce to 100-120 mmHg systolic
* Beta blockers are the first-line management
o Labetalol
* Nitroprusside
Differentiate between thrombus and embolus
Thrombus
* Blood clot results from ruptured atherosclerotic plaque or stagnant blood flow from cardiac arrhythmia
* Occlusion of small, distal arteries
* History of peripheral artery disease
Embolus
* A blood clot arising from the vascular system that travels to a distal area, causing occlusion
* Occlusion of larger arteries
* History of cardiac event
Clinical findings of arterial occulsion
Abrupt onset pain in extremity
The 5 P’s
o Pain
o Pulselessness
o Pallor
o Paralysis
o Paresthesia
o Limb is cool to touch
o Degree of ischemia is related to collateral blood flow
Arterial occlusion dx and tx
Dx – typically done off physical Exam Findings & Arterial/Venous Doppler Findings
Diagnostics:
* Vascular Sonography
* Arterial Doppler Ultrasound
* CT Angiography
* Delayed intervention
Tx
* Anticoagulation
* Unfractionated Heparin IV
* Catheter-directed thrombolysis
* tPA (Tissue plasminogen activator)
* Thromboembolectomy
* Revascularization must take place within 3 hours
Thrombophlebitis: RF, presentation, PE, Dx, Tx
Risk Factors: virchows triad (venous stasis, vascular injury, hyper coagulability)
Presentation:
o Dull pain
o Erythema
o Tenderness
o Palpable induration or cord
o Most common presentation on PANCE questions will be patient post trauma, or at IV/PICC site
Physical exam: erythema, tenderness, cord
Dx: Ultrasound: r/o deep vein involvement or occlusion
Treatment
o Rest
o Warm compresses, heat
o Elevation
o NSAIDS
